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  • Chemistry  (1)
  • GASTRIC MOTILITY  (1)
  • NITRIC OXIDE  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Gastric Motility and Mucosal Ulcerogenic Responses Induced by Rats Under Prostaglandin-Deficient Conditions Prokinetic Drugs in (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 251-258 
    Details
    ISSN: 1573-2568
    Keywords: PROKINETIC DRUG ; GASTRIC MOTILITY ; GASTRIC LESION ; PROSTAGLANDIN DEFICIENCY
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to examinewhether gastric prokinetic drugs may induce damage inthe rat stomach under normal and prostaglandin(PG)-deficient conditions. Male SD rats fasted for 18 hrwere administered subcutaneously with threedifferent prokinetic drugs such as metoclopramide (3-60mg/kg), ondansetron (0.3-3 mg/kg), and cisapride (3-30mg/kg). Half the number of these animals were pretreated with indomethacin (5 mg/kg) subcutaneously forinduction of PG deficiency in the stomach.Administration of these drugs increased gastric motoractivity in a dose-dependent manner and expeditedgastric emptying at lower doses than those affectinggastric motility; the potency of the hypermotilityeffect was in the following order: metoclopramide =ondansetron 〉 cisapride. None of these drugs alonecaused gross damage in the stomach, although whitishrough areas were observed in the gastric mucosa alongthe folds. In the rats pretreated with indomethacin,however, both metoclopramide and ondansetron provoked multiple hemorrhagic lesions in the gastricmucosa. Indomethacin at this dose showed over 90%inhibition of cyclooxygenase activity without causingany damage in the stomach, and this PG-deficient effect was not affected by coadministration with theprokinetic drugs. The mucosal ulcerogenic responsesinduced by metoclopramide in the presence ofindomethacin were significantly inhibited by prioradministration of atropine (1 mg/kg) or PGE2 (300μg/kg) at doses that inhibited gastric hypermotilityinduced by metoclopramide. These results suggest that:(1) gastric prokinetic drugs induce damage in ratstomachs under PG-deficient conditions at the doses that enhance gastric motility and emptying but notat the doses that expedite gastric emptying only, and(2) gastric hypermotility has the potential to causegross damage in the stomach, supporting the importance of gastric motility as a pathogenic element ofgastric lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018889129410
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanism of Acid Secretory Changes in Rat Stomach After Damage by Taurocholate Role of Nitric Oxide, Histamine, and Sensory Neurons (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 645-653 
    Details
    ISSN: 1573-2568
    Keywords: STOMACH ; TAUROCHOLATE ; BARRIER DISRUPTION ; ACID SECRETION ; NITRIC OXIDE ; HISTAMINE ; SENSORY NEURON
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to investigatethe mechanism underlying the acid stimulatory responsein the stomach after damage under the inhibition ofnitric oxide (NO) production byNG-nitro-L-arginine methyl ester (L-NAME). A rat stomach wasmounted in an ex vivo chamber, perfused with saline, andthe potential difference (PD) and acid secretion weremeasured before and after the application of 20 mM taurocholate (TC) for 30 min. Exposure of thestomach to TC caused a PD reduction and a decrease ofacid secretion. Pretreatment with L-NAME did not affectbasal acid secretion but significantly enhanced the acid secretion in the stomach after damagewith TC, without any effect on the PD response. Thiseffect of L-NAME was antagonized by simultaneousadministration of L-arginine but not D-arginine. The luminal appearance of NO was significantlyincreased in the stomach after exposure to TC, and thischange was completely blocked in the presence of L-NAMEor when EGTA was applied together with TC. The enhanced acid secretory response to TC in thepresence of L-NAME was inhibited by pretreatment withcimetidine, FPL-52694 (a mast cell stabilizer), orspantide (a substance P antagonist) or by chemical ablation of capsaicinsensitive sensory neurons.Mucosal exposure to TC increased histamine output in thelumen and decreased the number of metachromaticallystaining cells in the stomach, and these changes were also significantly prevented by FPL-52694,spantide, or sensory deafferentation. These resultssuggest that 1) damage in the stomach may activate theacid stimulatory pathway in addition to the NO-dependent inhibitory mechanism, but the latter effectovercomes the former, resulting in a decrease in acidsecretion, 2) the acid stimulation in the damagedstomach may be mediated by histamine released from the mucosal mast cell which may interact withcapsaicin-sensitive sensory nerves, and 3) L-NAMEunmasks the acid stimulatory response by suppressing theinhibitory mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018875932503
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Biocoulometry of cholesterol using porous carbon felt electrodes (1991)
    Weinheim : Wiley-Blackwell
    Electroanalysis 3 (1991), S. 59-62 
    Details
    ISSN: 1040-0397
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Free and total cholesterols in human serum have been determined by controlled-potential coulometry with porous carbon felt electrodes. In such a coulometric cell, a small amount of sample solution was dropped on the carbon felt dipped into electrolyte containing enzymes and a mediator. Hydrogen peroxide is produced by the enzymatic reaction of cholesterol catalyzed by cholesterol oxidase, and the complete electroreduction of hexacyanoferrate(III) ions [produced by the reaction of hexacynoferrate(II) ions and hydrogen peroxide catalyzed by peroxidase] was carried out under controlled-potential conditions. In the case of determining total cholesterol in human serum, cholesterol esters were converted to free cholesterol by cholesterol esterase reaction prior to the addition of the sample solution into electrolyte. The conversion ratios of free cholesterol to hydrogen peroxide were found to be 85-89% (RSD 〈 6%). The electrolysis time of one sample was less than 5 minutes. Immobilization of cholesterol oxidase to the carbon felt surface was attempted; the activity of cholesterol oxidase, Immobilized by the diazo-coupling method began to decrease 3 days after the immobilization.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/elan.1140030111
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    Paper (German National Licenses)
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